Respiratory System (Gas Exchange (Diffusion (Rate of Diffusion (Fick's…
- To provide O2 to the body
- To eliminate CO2
- Short term regulation fo the pH of blood.
- Defense against mirobes
- Trapping and dissolving of clots
- Body heat and water loss
Lungs and Pleura:
- Each lung surrounded by a pleural sac.
- Pleural sacs separated by space filled with intrapleural fluid.
- Fluid allows the free movement of the lungs in the cavity that direct attachment wouldn't.
- 23 divisions
- Radius decreases with branching but cross sectional area increases so resistance overall decreases.
- Gas Echange
- Gas Exchange
- Cellular Respiration
- Total gas flow into the lungs per minute
- Tidal volume x frequency of breathing
- Deep Slow Breathing: Increased alveolar ventilation
- Breathing through snorkel: Same as normal breathing
- Fast and Shallow Breathing: Decreased alveolar ventilation
Mechanics of Breathing:
- Lungs have elastic elements exerting an elastic recoil inwards.
- Chest wall has elasticity exerting outwards recoil.
- Generates a negative pressure within the pleural space (suction) which means the lungs expand as the chest wall does.
- Transpulmonary pressure = force acting to expand the lungs
- Inspiratory intercostal muscles contract
- Thorax expands
- Pip changes from -4 to -7
- Ptp increases from 4 to 7 (lungs expand)
- Palv changes from 0 to -1 at mid inspiration
- Palv is less than Patm so air moves into the lungs
- At the end of inspiration Palv = 0mmHg
- Passive process requiring no muscle contraction, just elastic recoil.
- Inspiratory muscles relax
- Thorax shrinks pulled by elastic recoil of the lungs
- Pip rises from -7 to -4
- Palv rises from 0 to +1 mid expiration
- Palv is greater than Patm so air flows out of the lungs
- 500mL = tidal volume
- 3L = inspiratory reserve volume
- 1.2L = expiratory reserve volume
- 1.2L = residual volume
- 4.7L = vital capacity
- 5.9L = total lung capacity
- 150mL = anatomic dead space
- Alveolar dead space = volume where alveoli are inadequately perfused with blood. Reduces gas exchange.
- Physiological dead space = anatomical dead space + alveolar dead space
- Easily distensible
- Small pressure change leads to a large volume change.
- Elastic recoil is reduced, expiratory muscle activity may be required for quiet breathing
- Easy to inflate
- Difficult to inflate the lungs
- Elastic recoil is high, passive recoil of lungs during expiration is not a problem
- Pulmonary fibrosis (restrictive lung disease), inspiration is difficult. Shallow rapid breaths are normally taken as a result.
Elastic elements in the alveolar insterstitium
- The more elastic fibres the greater resistance to stretching
Surface tension between air and fluid layer
- Accounts for 75% of the elastic recoil of the lungs
- Water molecules are attracted to each other across the alveoli pulling it inwards favouring collapsing due to surface tension.
- Surfactant acts as a detergent creating a layer between the molecules and therefore increases lung compliance
- Respiratory distress syndrome: type II alveolar cells are too immature to secrete surfactant and energy required to overcome the surface tension and inflate the alveoli is too exhausting
- Viscosity of air
- Length (fixed)
- Diameter/radius. R = 1/r4
- Gas molecules undergo continuous random motion which exerts a pressure.
- Dependent on concentration and temp.
- Because gas molecules are so far apart they do not normally interfere with each other so exert their own partial pressure.
- Net diffusion = area of high PP to low PP
- Exerts a pressure equivalent to 47mmHg at 37 degrees
- Alveolar PO2 is lower than that of PInspired as some O2 leaves via the pulmonary capillaries
- Equation: PA(O2) = PI(O2) - (VO2/VA x 863)
- Increase VO2 = decrease PAO2
- Increase PIO2 = increase PAO2
Alveolar Carbon Dioxide
- Increase VCO2 = increase PACO2
- Increase PICO2 = increase PACO2
- Diffusion of gases in a liquid is proportional to the relative partial pressures .
- Gives rise to gas exchange in the lungs between capillaries and alveoli.
- When equip is reached diffusion stops.
- In a healthy person, is extremely rapid.
- Due to diffusion properties of O2 and CO2, the thin walls of the alveoli and the large alveolar surface area over which gas diffusion can occur
Rate of Diffusion
Directly related to:
- Partial pressure difference
- SA over which diffusion is occuring
- Diffusion constant for the gas
- Inversely related to the thickness of the barrier
Diffusion constant much greater for CO2 as it more soluble in plasma. Has potential to be much faster but has a lower gradient so in reality is not.
- Pulmonary Oedema: fluid leaks out of capillaries into interstitial space.
- Interstitial Fibrosis: thickening of the alveolar wall
- Emphysema: reduces surface area, reduces the number of capillaries.
Oxygen in Blood
- 1.5% physically dissolved
- 98.5% bound to hemoglobin
- Concentration = 150g/L
- Each gram saturated = 1.34mL of O2
- Max = 201mL O2/L of Blood
- Amount bound is determined by the PO2 in the blood
- Percent O2 saturation arterial blood = 98%
- Percent O2 saturation venous blood = 75%
- Has a steep slope between PO2 of 10-60mmHg
- Steepness = large quantities of O2 can be off-loaded from Hb with only a small decrease in PO2
- Plateau = flat portion between PO2 of 60-120mmHg
- Plateau = blood retains a good saturation even if alveolar PO2 and thus arterial PO2 were to fall dramatically e.g. at high altitude or with lung disease.
Affinity of Hb for O2
- Assessed at PO2 where it is 50% saturated.
- P50 of arterial blood = 25mmHg
- Anything that increases the affinity will cause a reduction in P50 as a lower partial pressure of O2 is required for the Hb to become saturated.
- Leads to leftward shift of dissociation curve or LOADING
- Known as the Bohr Effect
- Any factor that decreases the affinity will increase P50 as a higher partial pressure of O2 is required to reach 50% saturation.
- Leads to rightward shift of curve
- Facilitates the release of O2
- Known as the Bohr Effect
- Increase PCO2 and decreasing pH (increasing H+ concentration) and temperature causes RIGHT shift of curve as it reduces the affinity of Hb for O2
- DeoxyHb has greater H+ affinity. Binds most of the H+ ions produced by metabolism
- When blood passes through the lungs all reactions are reversed, H+ dissociated as binds with bicarbonate.
Carbonic Acid - Bicarbonate:
- Very efficient
- Increase in [H+] drives the reaction to the left.
- H2CO3 is produced which produces CO2 and H2O
- Excess CO2 released in alveoli
- A fall in [H+] drives the reaction to the right, less CO2 is released in expiration
- Reduced blood pH
- Increased H+
- Hypoventilation leads to retention of CO2 in blood
- Increased CO2 will drive the reaction to the right, increasing the H+ produced and thus acidosis.
- Increased blood pH
- Decreased H+
- Hyperventilation will lead to increased loss of CO2
- Drives reaction to the left which reduces H+ produced and therefore pH rises.
- Decrease alveolar ventilation = hypoventilation
- Increase alveolar ventilation = hyperventilation
- Lung diseases like emphysema and bronchitis/asthma
- Decreased airflow = body responds by decreasing blood flow (vasoconstriction)
- Decreased blood flow = body responds by decreasing alveolar flow (bronchoconstriction)
- Dissolved in the plasma and cytoplasm of RBC's 10% (only CO2 responsible for blood PCO2).
- Bound reversibly to Hb forming carbamino compounds (30%)
- As bicarbonate ions (60%)
- Bound to amino groups
- CO2 + Hb <=> HbCO2
- Conversion occurs in the erythrocytes
- Catalysed by carbonic anhydrase
- Most bicarb moves into the plasma
- CO2 + H2O produces 2 osmotically active particles, H+ and HCO3
- HCO3 moves out of RBC down gradient
- Cl- moves into RBC to maintain neutrality
- H2O moves into RBC to maintain osmolarity
- Blood PCO2 is higher than alveolar PCO2 so CO2 diffuses from plasma into the alveoli
Blood Dissociation Curve + The Haldane Effect:
- Not Hb, all forms of CO2 transport in blood make up the curve
- When PO2 is low, the curve shifts to the left, CO2 binds more readily to globin.
- Facilitates removal of CO2 from tissues, advantage to venous blood.
- When PO2 is high, the curve shifts down, CO2 binds less readily to the globin as O2 binding causes shape change that makes it harder.
- Facilitates the release of CO2 (i.e. in pulmonary capillaries) as blood picks up more oxygen.
Involuntary Control: Inspiratory
- Respiratory muscles do not contract spontaneously
- Breathing pattern is generated involuntarily in the resp centres of the medulla oblongata.
- Neurons in the inspiratory spontaneously discharge, initiate APs to motor neurons which initiates muscle contraction.
- Spontaneous discharge is limited in duration
- Can voluntarily control our breathing patterns etc using the cerebral cortex.
- Cerebral cortex sends signals directly to the respiratory muscles' motor neurons in spinal cord, bypasses respiratory centres.
Involuntary Control: Expiratory
- Neurons in expiratory centre are normally quiescent.
- Expiratory centre only fires when expiratory muscle activity is required - forced expiration.
Sensory Input: Nucleus Tractus Solitarius
- Sensory input to respiratory centres via mechanoreceptors, chemoreceptors etc.
- Cause reflex adjustments in breathing response.
- Irritation of nasal mucosa stimulates mechanoreceptors
- Sneeze response (high velocity expiration) removes the irritant
- Mechanoreceptors in larynx stimulated by irritant
- long slow inspiration followed by rapid powerful expiration against closed glottis helps remove irritant
- Breathing adjusted automatically to maintain PO2, PCO2 and [H+]
- Arterial gases = altered by alveolar ventilation
- Arterial blood = closely monitored by chemoreceptors
- Peripheral: Caroitd bodies (bifurcation of common carotid) and Aortic bodies (aortic arch).
- Input travels via glossopharyngeal nerve and vagus nerve
- Decrease in PO2 (hypoxia)
- Increase in arterial PCO2 (hypercapnia)
- Increase in arterial H+ (acidosis)
= Causes an increase in ventilation.
- Insensitive to hypoxia + arterial acidosis (because H+ ions cannot pass the blood brain barrier)
- Concentration of H+ in the brain ECF
- Source of H+ ions at central chemoreceptors = CO2 (can cross barrier) CO2 is converted into HCO3- and H+ once in the ISF.
- Respons = increased ventilation.
- Medullary respiratory centres increase the rate of ventilation
- Moves PO2 of alveolar air and PO2 of arterial blood back towards normal.
- Not stimulated until arterial PO2 reaches 60mmHg
- Minute ventilation vs PO2 mmHg
- Increase PCO2 leads to increased arterial H+
- Increases firing, leads to increased ventilation
- Less prominent effect than central
- Most important response mechanism (70%)
- CO2 rapidly diffuses across barrier
- Increases H+ in ISF of medulla
- Stimulate chemoreceptors and increases ventilation.
- Evens small changes leads to large increase in ventilation - steep curve, no plateau.
- Increase H+ concentration (e.g. lactic acid)
- H+ ions don't pass blood brain barrier
- Signal is sent to the medullary respiratory centres
- Ventilation is increased (hyperventilation)
- Leads to CO2 being blown off to decrease CO2 and therefore decrease H+ concentration.
- Metabolic alkalosis loss of H+ ions e.g. vomitting increases pH
- Reduced [H+] is detected by peripheral chemoreceptors and ventilation is reduced. (Hypoventilation)
- Increase PCO2
- Increases H+ ions